Predicting the possible effect of miR-203a-3p and miR-29a-3p on DNMT3B and GAS7 genes expression
Author:
Ali Afgar1, Mahla Sattarzadeh Bardsiri234, Reza Vahidi1, Alireza Farsinejad34
Affiliation:
1. Research Center for Hydatid Disease in Iran , Kerman University of Medical Sciences , Kerman , Iran 2. Student Research Committee, Faculty of Allied Medicine , Kerman University of Medical Sciences , Kerman , Iran 3. Department of Hematology and Medical Laboratory Sciences, Faculty of Allied Medicine , Kerman University of Medical Sciences , Kerman , Iran 4. Cell Therapy and Regenerative Medicine Comprehensive Center , Kerman University of Medical Sciences , Kerman , Iran
Abstract
Abstract
Aberrant expression of genes involved in methylation, including DNA methyltransferase 3 Beta (DNMT3B), can cause hypermethylation of various tumor suppressor genes. In this regard, various molecular factors such as microRNAs can play a critical role in regulating these methyltransferase enzymes and eventually downstream genes such as growth arrest specific 7 (GAS7). Accordingly, in the present study we aimed to predict regulatory effect of miRNAs on DNMT3B and GAS7 genes expression in melanoma cell line. hsa-miR-203a-3p and hsa-miR-29a-3p were predicted and selected using bioinformatics software. The Real-time PCR technique was performed to investigate the regulatory effect of these molecules on the DNMT3B and GAS7 genes expression. Expression analysis of DNMT3B gene in A375 cell line showed that there was a significant increase compared to control (p value = 0.0015). Analysis of hsa-miR-203a-3p and hsa-miR-29a-3p indicated the insignificant decreased expression in melanoma cell line compared to control (p value < 0.05). Compared to control, the expression of GAS7 gene in melanoma cells showed a significant decrease (p value = 0.0323). Finally, our findings showed that the decreased expression of hsa-miR-203a-3p and hsa-miR-29a-3p can hypothesize that their aberrant expression caused DNMT3B dysfunction, possible methylation of the GAS7 gene, and ultimately decreased its expression. However, complementary studies are necessary to definite comment.
Publisher
Walter de Gruyter GmbH
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